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‫بسم ا الرحمن الرحيم‬
GENERA:
TREPONEMA & BORREILIA
Prof. Khalifa Sifaw Ghenghesh
 Unicellular

helical or spiral rodshaped spirochaetes.
 Actively motile
– Flagella attached at each pole of the
cell and wrap around the bacterial
cell body
– Flagella are enclosed within the
bacterial outer membrane
Treponema
Do not stain by Gram’s method
 Pathogenic Treponema


–
–
–
–

T.
T.
T.
T.

pallidum
pertenue
endemicum
carateum

– Cannot be cultivated in laboraotry media
– Maintained by subculture in susceptible
animals
– Differentiation of organisms is based
primarily on clinical syndromes
– Micro-aerophilic
Treponema pallidum
 Syphilis

– Acquired by sexual contact with
infected person
 Congenital

Syphilis

– Infected mother to fetus in utero or
during passage of neonates through
infected canal (vertical
transmission)
PATHOGENESIS
Untreated the disease may progress
to Primary, Secondary, latent and
Tertiary stages.
 Primary syphilis


– Organism penetrates intact mucosae >
lymphatics > disseminates via blood to
any organ
– Multiplies at entry site > ~ 3 weeks >
painless chancre (mainly on external
genitalia).
– Chancre heals spontaneous in 3-6 weeks


Secondary syphilis
– Appear 2-12 weeks
– Symptoms are highly variable but mainly
involve the skin (macular or pustular
lesion)
– Lesions are highly infectious and
gradually resolve



Latent syphilis
– No clinical manifestations are seen but
serological evidence of infection remains
– Individuals are not generally infectious
but can transmit infection to the fetus
during pregnancy
– Their blood can be infectious
 Tertiary

syphilis

– May develop decades after primary
syphilis
– A slowly progressive, destructive
inflammatory disease > affects any
organ
 Neurosyphilis
 Cardiovascular

syphilis
 Gummatous syphilis
Histopathology showing Treponema
pallidum spirochetes.
Modified Steiner silver stain.
Treponema pallidum
darkfield preparation
Light microscope pictures showing
tissue infected with the spirochete
Treponema pallidum, the causative
agent of syphilis.
Treponema organisms stained by
fluorescent-tagged antibodies.
Treponema pertenue
– Yaws
– Rural population in subtropical countries
– Non-venereal, after contact of traumatized skin
with exudate from early yaws lesion
– Primary yaws (3-5 weeks) > lesions on the legs
>> papular lesions >> enlarge erode and heal
spontaneously within 6 months > may erupt
weeks or months later.
– Secondary lesions > bones (fingers, long bones
and jaw)
– Late yaws > cutaneous plaques and ulcers and
thickening of the skin on the palms and soles of
the feet.


No neurological and cardiovascular damage

– No congenital yaws
Treponema endemicum
– Bejel (endemic syphilis)
– Non-venereal, affects mainly children rural
populations in Africa, western Asia and Australia
– Direct person to person contact and by sharing
contaminated eating and drinking utensils
– Initial lesion > oral
– Secondary lesions > oropharyngeal mucous
patches, condyloma lata and periostitis
– Late lesion > gummata in the skin, nasopharynx
and bones


No neurological and cardiovascular damage

– congenital bejel is rare
Treponema carateum
 Pinta

Rural regions of Mexico, Central
America and Colombia
 Confined to the skin
 Non-destructive lesion but cause
disfigurement
 Direct contact with infectious lesions
resulting in depigmented lesions
which are characteristic of late stages
of pinta with no serious harm

LABORATORY DIGNOSIS


Direct Microscopy

– Specimen: fresh exudate from primary
or secondary lesions
– Examine with dark-ground or phase
contrast microscopy


Serological Tests

- T. pallidum infection > 2 types of Abs
– Specific Abs against polypeptide Ags of
the bacterium
– Non-specific Abs reacts with a nontreponemal Ag > Cardiolipin
1. Non-Specific Serological Test


The Venereal Disease Reference
Laboratory (VDRL) Test

- Mixture of Cardiolipin, cholestrol and licithin as Ag

- IgM or IgG Ab in positive serum or CSF
from neurosyphilis case causes a
suspension of lipoidal Ag to flocculate >
read by the eye
- Used as a screening test >
– 70% of primary and 99% of secondary syphilis
cases are positive
– Negative in late syphilis

- Quantitatively > diagnosis of congenital syphilis
- To monitor the efficacy of antibiotic therapy
2. Tests for Specific Antibody
i. Fluorescent treponemal Ab (FTA-Abs) test
– Indirect immunofluorescence assay
– T. pallidum = Ag
– Acetone-fixed treponemes incubated with heattreated sera > bound Ab detected by
fluorescin-labelled conjugate and UV
microscopy
– Positive in 80% primary, 100% secondary and
95% late syphilis patients.
– Remain positive after treatment
ii. T. pallidum haemagglutination assay (TPHA)
- RBCs coated with T. pallidum Ag
- Specific Ab in test sera >> haemaggluination
- Positive in 65% primary, 100% secondary and
95% late syphilis patients.
-Remains positive for life
iii. Other Antibody tests
- Monoclonal ant-T. pallidum Abs > ELISA
- Detects Ab response individual treponemal Ags
- Rapid screening of large number of samples
TREATMENT
 Primary

and Secondary Syphilis

– Prolonged high dose of procaine
penicillin
– Erythromycin, tetracycline or
choramphenicol
 Late

Syphilis

– Aqueous benzylpenicillin
CONTROL
 Treating

index cases and any
known contacts
Borrelia
 Gram-negative
 Cause

Relapsing fevers
 Transmitted by arthropod vectors
 Characterized clinically by
recurrent periods of fever and
spirochaetaemia
 Disease occur world-wide
Borrelia recurrentis
 Cause

epidemic or louse-borne
Relapsing fever
– An obligate human pathogen
– Person-to-person transmission by
the body louse Pediculus humanus
Other Borrelia
B. duttoni
 B. hermsii
 B. parkeri
 B. turicatae
 Cause endemic or thick-borne
relapsing fever
 Transmitted to humans by soft-bodied
Ornithodorus ticks
 Natural hosts


– Rodents and other small mammals
LABORATORY DIAGNOSIS
 Specimen

– Peripheral blood
 Thick

or thin blood smears
stained with Giemsa, acridine
orange or other stains
 Serological tests
– Not reliable (due to antigenic
variation) and not widely available
TREATMENT AND CONTROL
 Tetracycline,

Erythromycin,
chloramphenicol and penicillin
 Prevention
– Avoidance or eradication of the
insect vector
– Eradication of ticks from human
dwellings using insecticides
– Louse-borne infection
 Good

personnel hygiene
 If necessary >> delousing

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Lecture 27 Treponema and Borrelia

  • 1. ‫بسم ا الرحمن الرحيم‬ GENERA: TREPONEMA & BORREILIA Prof. Khalifa Sifaw Ghenghesh
  • 2.  Unicellular helical or spiral rodshaped spirochaetes.  Actively motile – Flagella attached at each pole of the cell and wrap around the bacterial cell body – Flagella are enclosed within the bacterial outer membrane
  • 3. Treponema Do not stain by Gram’s method  Pathogenic Treponema  – – – – T. T. T. T. pallidum pertenue endemicum carateum – Cannot be cultivated in laboraotry media – Maintained by subculture in susceptible animals – Differentiation of organisms is based primarily on clinical syndromes – Micro-aerophilic
  • 4. Treponema pallidum  Syphilis – Acquired by sexual contact with infected person  Congenital Syphilis – Infected mother to fetus in utero or during passage of neonates through infected canal (vertical transmission)
  • 5. PATHOGENESIS Untreated the disease may progress to Primary, Secondary, latent and Tertiary stages.  Primary syphilis  – Organism penetrates intact mucosae > lymphatics > disseminates via blood to any organ – Multiplies at entry site > ~ 3 weeks > painless chancre (mainly on external genitalia). – Chancre heals spontaneous in 3-6 weeks
  • 6.  Secondary syphilis – Appear 2-12 weeks – Symptoms are highly variable but mainly involve the skin (macular or pustular lesion) – Lesions are highly infectious and gradually resolve  Latent syphilis – No clinical manifestations are seen but serological evidence of infection remains – Individuals are not generally infectious but can transmit infection to the fetus during pregnancy – Their blood can be infectious
  • 7.  Tertiary syphilis – May develop decades after primary syphilis – A slowly progressive, destructive inflammatory disease > affects any organ  Neurosyphilis  Cardiovascular syphilis  Gummatous syphilis
  • 8. Histopathology showing Treponema pallidum spirochetes. Modified Steiner silver stain.
  • 10. Light microscope pictures showing tissue infected with the spirochete Treponema pallidum, the causative agent of syphilis.
  • 11. Treponema organisms stained by fluorescent-tagged antibodies.
  • 12. Treponema pertenue – Yaws – Rural population in subtropical countries – Non-venereal, after contact of traumatized skin with exudate from early yaws lesion – Primary yaws (3-5 weeks) > lesions on the legs >> papular lesions >> enlarge erode and heal spontaneously within 6 months > may erupt weeks or months later. – Secondary lesions > bones (fingers, long bones and jaw) – Late yaws > cutaneous plaques and ulcers and thickening of the skin on the palms and soles of the feet.  No neurological and cardiovascular damage – No congenital yaws
  • 13. Treponema endemicum – Bejel (endemic syphilis) – Non-venereal, affects mainly children rural populations in Africa, western Asia and Australia – Direct person to person contact and by sharing contaminated eating and drinking utensils – Initial lesion > oral – Secondary lesions > oropharyngeal mucous patches, condyloma lata and periostitis – Late lesion > gummata in the skin, nasopharynx and bones  No neurological and cardiovascular damage – congenital bejel is rare
  • 14. Treponema carateum  Pinta Rural regions of Mexico, Central America and Colombia  Confined to the skin  Non-destructive lesion but cause disfigurement  Direct contact with infectious lesions resulting in depigmented lesions which are characteristic of late stages of pinta with no serious harm 
  • 15. LABORATORY DIGNOSIS  Direct Microscopy – Specimen: fresh exudate from primary or secondary lesions – Examine with dark-ground or phase contrast microscopy  Serological Tests - T. pallidum infection > 2 types of Abs – Specific Abs against polypeptide Ags of the bacterium – Non-specific Abs reacts with a nontreponemal Ag > Cardiolipin
  • 16. 1. Non-Specific Serological Test  The Venereal Disease Reference Laboratory (VDRL) Test - Mixture of Cardiolipin, cholestrol and licithin as Ag - IgM or IgG Ab in positive serum or CSF from neurosyphilis case causes a suspension of lipoidal Ag to flocculate > read by the eye - Used as a screening test > – 70% of primary and 99% of secondary syphilis cases are positive – Negative in late syphilis - Quantitatively > diagnosis of congenital syphilis - To monitor the efficacy of antibiotic therapy
  • 17. 2. Tests for Specific Antibody i. Fluorescent treponemal Ab (FTA-Abs) test – Indirect immunofluorescence assay – T. pallidum = Ag – Acetone-fixed treponemes incubated with heattreated sera > bound Ab detected by fluorescin-labelled conjugate and UV microscopy – Positive in 80% primary, 100% secondary and 95% late syphilis patients. – Remain positive after treatment
  • 18. ii. T. pallidum haemagglutination assay (TPHA) - RBCs coated with T. pallidum Ag - Specific Ab in test sera >> haemaggluination - Positive in 65% primary, 100% secondary and 95% late syphilis patients. -Remains positive for life iii. Other Antibody tests - Monoclonal ant-T. pallidum Abs > ELISA - Detects Ab response individual treponemal Ags - Rapid screening of large number of samples
  • 19. TREATMENT  Primary and Secondary Syphilis – Prolonged high dose of procaine penicillin – Erythromycin, tetracycline or choramphenicol  Late Syphilis – Aqueous benzylpenicillin
  • 20. CONTROL  Treating index cases and any known contacts
  • 21. Borrelia  Gram-negative  Cause Relapsing fevers  Transmitted by arthropod vectors  Characterized clinically by recurrent periods of fever and spirochaetaemia  Disease occur world-wide
  • 22. Borrelia recurrentis  Cause epidemic or louse-borne Relapsing fever – An obligate human pathogen – Person-to-person transmission by the body louse Pediculus humanus
  • 23. Other Borrelia B. duttoni  B. hermsii  B. parkeri  B. turicatae  Cause endemic or thick-borne relapsing fever  Transmitted to humans by soft-bodied Ornithodorus ticks  Natural hosts  – Rodents and other small mammals
  • 24. LABORATORY DIAGNOSIS  Specimen – Peripheral blood  Thick or thin blood smears stained with Giemsa, acridine orange or other stains  Serological tests – Not reliable (due to antigenic variation) and not widely available
  • 25. TREATMENT AND CONTROL  Tetracycline, Erythromycin, chloramphenicol and penicillin  Prevention – Avoidance or eradication of the insect vector – Eradication of ticks from human dwellings using insecticides – Louse-borne infection  Good personnel hygiene  If necessary >> delousing